Ancient viral genomes reveal introduction of human pathogenic viruses into Mexico during the transatlantic slave trade
Abstract
After the European colonization of the Americas there was a dramatic population collapse of the Indigenous inhabitants caused in part by the introduction of new pathogens. Although there is much speculation on the etiology of the Colonial epidemics, direct evidence for the presence of specific viruses during the Colonial era is lacking. To uncover the diversity of viral pathogens during this period, we designed an enrichment assay targeting ancient DNA (aDNA) from viruses of clinical importance and applied it to DNA extracts from individuals found in a Colonial hospital and a Colonial chapel (16th c. - 18th c.) where records suggest victims of epidemics were buried during important outbreaks in Mexico City. This allowed us to reconstruct three ancient human parvovirus B19 genomes, and one ancient human hepatitis B virus genome from distinct individuals. The viral genomes are similar to African strains, consistent with the inferred morphological and genetic African ancestry of the hosts as well as with the isotopic analysis of the human remains, suggesting an origin on the African continent. This study provides direct molecular evidence of ancient viruses being transported to the Americas during the transatlantic slave trade and their subsequent introduction to New Spain. Altogether, our observations enrich the discussion about the etiology of infectious diseases during the Colonial period in Mexico.
Data availability
Reconstructed genomes from this study are available in Genbank under accession number MT108214, MT108215, MT108216, MT108217. NGS reads used to reconstruct ancient viral genomes reported in this study are available in Dryad (https://doi.org/10.5061/dryad.5x69p8d2s).
-
Data from: Ancient viral genomes reveal introduction of human pathogenic viruses into Mexico during the transatlantic slave tradeDryad Digital Repository, doi:10.5061/dryad.5x69p8d2s.
Article and author information
Author details
Funding
Welcome Trust Sanger (208934/Z/17/Z)
- María C Ávila Arcos
PAPIIT-DGAPA-UNAM (IA201219)
- María C Ávila Arcos
Human Frontier Science (RGY0075/2019)
- María C Ávila Arcos
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: Permission to process these samples were provided by the INAH Archeology Council with numbers 401.1S.3-2018/1373 and 401.1S.3-2020/1310 for the Hospital San Jose de los Naturales and the Temple of Immaculate Conception (La Conchita), respectively.
Copyright
© 2021, Guzmán-Solís et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 6,645
- views
-
- 818
- downloads
-
- 30
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
The transatlantic slave trade introduced dangerous human pathogens into Mexico
-
- Genetics and Genomics
- Immunology and Inflammation
Systemic lupus erythematosus (SLE) is an autoimmune disease, the pathophysiology and genetic basis of which are incompletely understood. Using a forward genetic screen in multiplex families with SLE, we identified an association between SLE and compound heterozygous deleterious variants in the non-receptor tyrosine kinases (NRTKs) ACK1 and BRK. Experimental blockade of ACK1 or BRK increased circulating autoantibodies in vivo in mice and exacerbated glomerular IgG deposits in an SLE mouse model. Mechanistically, NRTKs regulate activation, migration, and proliferation of immune cells. We found that the patients’ ACK1 and BRK variants impair efferocytosis, the MERTK-mediated anti-inflammatory response to apoptotic cells, in human induced pluripotent stem cell (hiPSC)-derived macrophages, which may contribute to SLE pathogenesis. Overall, our data suggest that ACK1 and BRK deficiencies are associated with human SLE and impair efferocytosis in macrophages.